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Biochim Biophys Acta. 2012 Dec;1823(12):2237-42. doi: 10.1016/j.bbamcr.2012.09.002. Epub 2012 Sep 12.

Impaired c-src activation and motility defects in PEA3-null fibroblasts.

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  • 1Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Rd, Ottawa, ON, Canada K1H8M5.

Abstract

Null mutations in the pea3 allele compromise the capacity of mammary tumors to metastasize in MMTV-Neu/ErbB2/HER2 transgenic mice, indicating a motility defect in PEA3-null cells. Cellular and biochemical analyses of established PEA3-null fibroblasts show impaired motility and aberrant localization of adhesion proteins in spreading cells. Our results show that PEA3-/- cells express normal levels of key adhesion components, but that spreading PEA3-null cells fail to activate c-src and to downregulate phospho-FAK(Y397), suggesting that focal adhesion signaling is impaired. Supporting this, biochemical analysis revealed that adhesion complex-associated proteins such as p130Cas failed to undergo tyrosine phosphorylation and dissociated from the adhesion complex with delayed kinetics. Overall our data show that the motility defects observed in PEA3-null cells are due to altered adhesion signaling.

Copyright © 2012 Elsevier B.V. All rights reserved.

PMID:
22982417
[PubMed - indexed for MEDLINE]
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